Elsevier

The Lancet

Volume 359, Issue 9303, 26 January 2002, Pages 303-309
The Lancet

Articles
Pulmonary extravascular fluid accumulation in recreational climbers: a prospective study

https://doi.org/10.1016/S0140-6736(02)07496-2Get rights and content

Summary

Background

High altitude pulmonary oedema (HAPE) that is severe enough to require urgent medical care is infrequent. We hypothesised that subclinical HAPE is far more frequent than suspected during even modest climbs of average effort.

Methods

We assessed 262 consecutive climbers of Monte Rosa (4559 m), before ascent and about 24 h later on the summit 1 h after arriving, by clinical examination, electrocardiography, oximetry, spirometry, carbon monoxide transfer, and closing volume. A chest radiograph was taken at altitude.

Findings

Only one climber was evacuated for HAPE, but 40 (15%) of 262 climbers had chest rales or interstitial oedema on radiograph after ascent. Of 37 of these climbers, 34 (92%) showed increased closing volume. Of the 197 climbers without oedema, 146 (74%) had an increase in closing volume at altitude. With no change in vital capacity, forced expiratory volume in 1 s and forced expiratory flow at 25–75% of forced vital capacity increased slightly at altitude, without evidence of oedema. If we assume that an increased closing volume at altitude indicates increased pulmonary extravascular fluid, our data suggest that three of every four healthy, recreational climbers have mild subclinical HAPE shortly after a modest climb.

Interpretation

The risk of HAPE might not be confined to a small group of genetically susceptible people, but likely exists for most climbers if the rate of ascent and degree of physical effort are great enough, especially if lung size is normal or low.

Introduction

High altitude pulmonary oedema (HAPE) is a potentially fatal consequence of rapid altitude ascent, especially when ascent is accompanied by substantial exercise. The incidence of HAPE in the USA is often said to be 2–5%.1, 2 Although the altitudes of most ski and alpine areas in the USA are only between 8000 and 10000 feet (2400 to 3000 m), most lowlanders travel quickly to altitude and undertake intense activity. By contrast, much higher ascents of Himalayan or Andean peaks allow acclimatisation by means of gradual ascent. Thus, HAPE tends to be less frequent on well planned ascents to much greater heights, despite the greater degree of hypoxaemia. Consequently, HAPE, although well recognised, is thought to be relatively rare, whether at moderate or very high altitudes.

Consistent with the view that HAPE is uncommon are the constitutional differences between people who develop HAPE and those who do not. People who go on to develop HAPE have higher pulmonary artery pressures,3, 4, 5 smaller lungs,6, 7, 8, 9 and higher pulmonary artery wedge pressures during even normoxic sea level exercise than those who do not develop HAPE.6, 7 Epithelial sodium and water transport could also be compromised in these people.4 Thus, there is a general sense that in a small fraction of the population, genetic factors, which produce a symptomless sea level phenotype demonstrable nonetheless by physiological measurements, predispose to HAPE.

Clinically significant HAPE leads to symptoms that cause the patient to seek medical attention. Because some degree of shortness of breath, tachycardia, cough, and arterial oxygen desaturation are frequently experienced at altitude, and because most climbers are keen to pursue the activities for which they came to high altitude areas in the first place, lesser degrees of HAPE might well go unreported. Thus, if all degrees of severity of HAPE are considered, its incidence might be much higher than 2–5%. A suggestion that HAPE could be much more common comes from Operation Everest II, a chamber simulation of a Mount Everest climb. As the participants passed through 6100 m, all but one of the seven developed clinical evidence of HAPE with substantial pulmonary gas exchange defects.11 This effect was not seen at lower altitudes, and, more importantly, was also not seen at higher altitudes, when ascent was purposefully slower.10 The early data of Singh12 support this concept as well, with an approximate 15% incidence in soldiers functioning at altitudes above about 3000 metres.

The notion that HAPE results from mechanical disruption of the pulmonary blood:gas barrier due to high pulmonary vascular pressures13 suggests that the condition might be more frequent than previously thought, since most healthy people exercising in acute hypoxia develop high mean pulmonary artery pressures (often >4 kPa), and pulmonary wedge pressures (often >2 kPa).14 Thus, conditions consistent with mechanical failure of pulmonary capillaries might be common during heavy exercise, even at moderate altitudes.

We therefore postulated that, although the rate of severe, life-threatening HAPE is indeed low, subclinical degrees of pulmonary fluid accumulation might be far more frequent than currently believed in normal climbing circumstances. If subclinical oedema is relatively frequent, the margin of safety for further ascent and exercise at altitude might be small.

Section snippets

Study design

We designed a 2-week study on Monte Rosa (4559 m on the Swiss-Italian Border). We included all climbers who had ascended from the Italian side at Alagna, successfully reached the summit of the mountain, and had consented to the study. Climbers were examined immediately before commencing the ascent at Alagna, altitude 1200 m. This is the cable car base from which climbers are lifted to 3200 m in 30 min or so, most often in the early afternoon. Climbers then generally hike for 1–2 h to 3600 m and

Results

For the 262 climbers examined at both locations, mean weight was 72·2 kg (SD 10·6), age was 39·8 years (12·0), and height was 174 cm (14). The mean weight of the backpack was 11·3 kg (4·8) and the time taken for the ascent was 4·3 h (1·3). Mean FVC at Alagna was 4·74 L (0·90; 104·4% predicted [13·3]; FEV1 was 3·88 L (0·71 103·4% predicted [12·8%]), and FEV1/FVC was 82·1% (6·5; 102·2% predicted [7·7]). 30 climbers were current smokers and 17 had smoked in the past. 88 had been to altitudes over

Discussion

Our data do not dispute the low incidence of full-blown HAPE requiring emergency care and evacuation, which was seen in just one of our participants. However, we suggest that subclinical interstitial oedema arises in most recreational climbers to modest altitude.

Features of our study that enhance its power and strengthen conclusions include: the large number of participants; the paired study design comparing each participant with identical methods at low and high altitude; the field nature of

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